Preserved force control by the digits via minimal sparing of cortico-spinal connectivity after stroke.

The ability to regulate finger forces is critical for manipulating objects during everyday tasks but is impaired after damage to white matter tracts that transmit motor commands into the spinal cord. This study examines cortico-spinal connectivity required for force control by the digits after neurological injury. We report on a unique case of a stroke survivor who retained the ability to control finger forces at a level comparable to neurologically intact adults despite extensive loss of white matter volume and severely compromised transmission from cortical motor areas onto the final common pathway.

Adaptation in the spinal cord after stroke: Implications for restoring cortical control over the final common pathway.

Control of voluntary movement is predicated on integration between circuits in the brain and spinal cord. Although damage is often restricted to supraspinal or spinal circuits in cases of neurological injury, both spinal motor neurons and axons linking these cells to the cortical origins of descending motor commands begin showing changes soon after the brain is injured by stroke. The concept of 'transneuronal degeneration' is not new and has been documented in histological, imaging and electrophysiological studies dating back over a century.

Effects of noninvasive neuromodulation targeting the spinal cord on early learning of force control by the digits.

Aims: Control of finger forces underlies our capacity for skilled hand movements acquired during development and reacquired after neurological injury. Learning force control by the digits, therefore, predicates our functional independence. Noninvasive neuromodulation targeting synapses that link corticospinal neurons onto the final common pathway via spike-timing-dependent mechanisms can alter distal limb motor output on a transient basis, yet these effects appear subject to individual differences.

Force oscillations underlying precision grip in humans with lesioned corticospinal tracts.

Stability of precision grip depends on the ability to regulate forces applied by the digits. Increased frequency composition and temporal irregularity of oscillations in the force signal are associated with enhanced force stability, which is thought to result from increased voluntary drive along the corticospinal tract (CST). There is limited knowledge of how these oscillations in force output are regulated in the context of dexterous hand movements like precision grip, which are often impaired by CST damage due to stroke.

Electrical stimulation of the external ear acutely activates noradrenergic mechanisms in humans.

Background: Transcutaneous stimulation of the external ear is thought to recruit afferents of the auricular vagus nerve, providing a means to activate noradrenergic pathways in the central nervous system. Findings from human studies examining the effects of auricular stimulation on noradrenergic biomarkers have been mixed, possibly relating to the limited and variable parameter space explored to date.

Objective: We tested the extent to which brief pulse trains applied to locations of auricular innervation (canal and concha) elicit acute pupillary responses (PRs) compared to a sham location (lobe).

Corticospinal recruitment of spinal motor neurons in human stroke survivors.

Key Points: Muscle weakness after stroke results from damage to corticospinal fibres that structurally and functionally connect cerebral cortex to the spinal cord. Here, we show an asymmetry in corticospinal recruitment of spinal motor neurons that is linked to maximal voluntary output of hand muscles weakened by stroke. Spike timing-dependent plasticity of synapses between corticospinal and spinal motor neurons transiently reversed recruitment failures in some survivors.